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NEUROMUSCULAR CASE OF THE MONTH - NOVEMBER 1999
Acquired Myasthenia gravis in a
2 year old female spayed Golden Retriever Mix
Contributed by Dr. Paul Donovan
Whites Road Veterinary Clinic
Pickering, Ontario, Canada
Clinical History
"Maggie" presented 12/2/98 for a second opinion for a recent onset of collapsing and ptyalism. She was healthy
until presentation for this problem.
Physical examination
Physical examination revealed "Maggie" to be bright and alert with normal temperature, pulse, respiration, and
capillary refill times. Neurological evaluation including cranial and spinal nerves was considered normal. The dog was weight
bearing on all 4 limbs but collapsed when she attempted to walk. A polyarthropathy or a motor unit disorder affecting the neuromuscular
junction was suspected.
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Diagnostic Tests
12/2/98 - The CBC was normal. The only abnormality found on the serum chemistry profile was an elevated cholesterol (16.6
mmol/l; reference 3.0-9.9 mmol/l). Pelvic and stifle radiographs were normal.
12/4/98 - Joint taps revealed a fair to good mucin clot test. Cytology showed a mild, non-suppurative degenerative joint disease. Culture
and sensitivity were negative. A non-articular cause to the locomotor problems could not be ruled out.
12/5/98 - Acetylcholine receptor antibody test submitted. A clinical trial of prednisone (40 mg SID) was initiated.
12/7/98 - Weakness progressed with groaning and now regurgitation
12/8/98 - A lateral chest radiograph revealed a megaesophagus. A Tensilon test (5 mg IV) revealed a dramatic positive response. Mestinon
therapy was initiated (60 mg BID) and the prednisone dosage was lowered to 30 mg SID.
12/10/98 - Thyroid evaluation supported primary hypothyroidism.
T3 - 2.30 (1.15-3.10 nmol/l)
T4 - <5.0 (19.0-58.0 nmol/l)
TSH - 1.70 (0.04-0.35 ng/ml)
T3 autoantibodies - 2.1 (0.0-2.0)
T4 autoantibodies - 0.6 (0.0-2.0)
Free T3 - 9.49 (2.00-4.60 pmol/l)
Free T4 - <5.0 (12.0-45.0 pmol/l)
12/21/98 - Acetylcholine receptor antibody titer (7.18 nmol/l; canine reference <0.6 nmol/l) diagnostic of acquired myasthenia gravis.
Treatment
Thyroid supplementation was initiated (12/10/98), Mestinon therapy was continued, and the prednisone dosage was further
decreased to 15 mg SID. The dog was clinically improving in muscle strength and regurgitation was decreased. A bout of colitis began
1/8/99 that was treated with Tylocin tablets. The prednisone dosage was further decreased to 5 mg every other day. A lateral chest
radiograph was repeated 1/22/99 that showed resolution of the megaesophagus. Since the megaesophagus was resolved, an attempt
was made to lower the Mestinon dosage to 60 mg SID but the dog began to "walk on eggshells" so the dosage was returned to
60 mg BID. The colitis continued and therapy was changed to Tylan powder. "Maggie" was maintained on thyroid supplementation,
Mestinon and colitis management over the next 7 months. By 9/15/99 the free T4 was within the normal range as was the acetylcholine
receptor antibody titer (0.13 nmol/l). Mestinon and prednisone therapy were stopped. As of 11/3/99 she was doing great, her myasthenia
gravis was in spontaneous remission, hypothyroidism under control and she was described as better than ever.
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Comment by Dr. Shelton
This case of acquired canine myasthenia gravis is an excellent example of how an early and correct diagnosis, appropriate therapy,
and recognition of other concurrent problems (in this case hypothyroidism) can result in a good clinical outcome. Acquired canine myasthenia
gravis still has an unacceptably high mortality rate (approximately 50%) and this is due in large part to misdiagnosis of vomiting
when in reality the dog is regurgitating due to esophageal dilatation. This delayed recognition usually involves inappropriate therapy
with an increase in the chance of developing an aspiration pneumonia which in itself may be life threatening. Our December
Special Feature will highlight several commonly asked questions regarding the diagnosis and treatment of myasthenia gravis.
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